When we last left off, our patient was a 63 year old male complaining of substernal chest pain which awoke him from sleep. We obtained standard, right-sided, and posterior ECG's which cardiology deemed non-specific. Our patient continued to have persistent chest pain even after maximal therapy.

Coronary catheterization was performed later that morning, and a total occlusion of the first obtuse marginal (OM1), a branch of the circumflex artery, was found. A drug eluting stent was placed, and his subsequent hospital course was unremarkable.

Could we have guessed this from the start? Let's take a look at his ECG's again:

Reviewing our patient's first ECG we see horizontal ST segment depression of 1 mm was seen in II and aVF, 3 mm ST depression in V2, and 1 mm ST depression in V3 and V4, all with upright T waves. An early R-wave transition was noted, with a height of 13 mV and an R/S of 1 in V2. Lead III showed T wave inversion.

The right-sided ECG featured only ST segment depression and inverted T-waves.

Reviewing the posterior leads, we see some interesting changes. Notably ST segment elevation of 0.5 mm in V7 and V8, and an unchanged appearance of the limb leads.

So, Dr. Walsh, what can we take away from this case?

Devoted readers of EMS 12-Lead will already know much about posterior MI, so I'll just do a brief review of the basics. I encourage you to search for the tag "posterior STEMI" for more information. As always, Dr. Stephen Smith's website also has plenty of examples and teaching about posterior MIs.

There is a small amount of controversy about what anatomic area of the heart a "posterior" MI actually affects. Some have suggested that the infarct is actually in the infero-basal region, while others have evidence that it should be viewed as a lateral infarct.

Regardless of the name, however, it generally is the result of an occlusion of the left circumflex coronary artery (link to cool animation). This territory is generally regarded as "electrically silent" in the standard ECG leads. As such, diagnosis relies on indirect evidence in the standard leads, as well as the use of non-standard "posterior" ECG leads.

So, how can we be Posterior STEMI Rock Stars, Doc?

For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:

Horizontal ST depression in V1-V4

Tall, broad R waves (>30ms)

Upright T waves

Dominant R wave (R/S ratio > 1) in V2

So, a typical posterior STEMI looks like this:

Inferioposterior STEMI courtesy of LifeInTheFastLane.

Note the ST elevations in the inferior and lateral leads; in general, a posterior MI usually shows signs of a STEMI in either of these two regions the majority of the time. It's pretty obvious that evidence of STEMI in one area (e.g. inferior) certainly strengthens suspicion for a posterior MI.

However, here's an example of a posterior MI that does not show any inferior or lateral involvement:

Using posterior leads (V7-V9) can show ST elevation, but the magnitude may not be as dramatic as that seen in the "usual" STEMIs. Many experts consider, for example, 0.5 mm of elevation to be significant, instead of the usual > 1 mm criteria, and that elevation in just one lead is sufficient.

So what's wrong with the conventional thinking?

There's a short-cut way to diagnose a posterior MI, that involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.

For example, a blow-up of lead V2 from the isolated posterior MI above (the second ECG) looks like this:

It fulfills all the criteria I reviewed above, so it's a classic example of how we currently define a posterior MI. And if we "flip" it, we get this:

Yep Doc, that looks like a regular STEMI now!

For many people (MDs included!), the diagnosis of a posterior MI starts, and ends, with this flipping.

I'll tell you what has always bothered me though. Look at the R-wave in the un-flipped image. This is just the mirror image of the Q-wave, and our "flipped" image reinforces that. In fact, the Q-wave in our flipped image looks pretty darn old, like the MI has progressed far along already.

Furthermore, the T-wave in our "flipped" image hardly looks hyper-acute. In fact, it looks like the T-waves are in the process of returning to baseline, another indication that our "classic" posterior MI is old.

Here's an example of an subacute/old inferior MI, for comparison. Also note the resolving, partially inverted, T-waves in III and aVF:

Old Inferior MI courtesy of LifeInTheFastLane.

It looks instead like our description of posterior MI is training us to look for old, completed MIs!

That's a classic STEMI, no doubt. Tiny Q-waves, tall T-wave – everything suggests that this is very acute.

Now, instead of being lead aVF, let's pretend it were lead V9. What would the "flipped" view of this lead be? Let's flip it and see!

This view shows a small R-wave, and a fully inverted and deep T-wave. Now, if we take a look back at the criteria listed above for a posterior MI, however, it would not meet much of the description of a posterior MI we listed before.

We're teaching people to pick up on old posterior MIs, and training them to miss the acute presentations.

5 Comments

Paramedics are suppose to be able to activate the cath-lab for anything they feel warrants it. It is suppose to allow us to completely bypass the ED all together.
The problem lies in that we call the ED to do this. So oftentimes there is a breakdown in communication and the patient ends up in a room in the ED instead, getting an EKG, and THEN the cath lab get activated, this sometimes happens for patients who are having a text book STEMI, not just a slightly wonky EKG.

I've been looking at a lot of these cases recently (my own, published lit, and posted online), and I really think there's more to the increased R/S ratio in V2 than just mirrored posterior Q-waves. There's something unique about the predominantly horizontal ST-depression seen with posterior STEMI as well.
I've just come across too many cases where the patient was clearly experiencing an acute MI, with symptoms for a hour or less (one as short as 20min), but they still often exhibited impressive R-waves in V2 with horizontal ST-depression. Performing the mirror trick, I agree that the complexes in those cases have a subacute morphology, but there's almost no way these patients have "completed" their infarcts so quickly. There must be something else at play, unique to the relationship between the QRS, ST, and T-wave and vectors in the Z-plane and the views of the heart offered by the precodial leads.

Also Dr. Walsh, do you think you can shoot me an email with that last paper? If you don't have my address, Christopher does. It sounds like its authors are trying to push that last 12-lead as being a quintessential acute posterior STEMI, but I'm interested in what else they have to say about it. Maybe there's something to the argument that a well developed R-wave in V2 is indicative of late infarct (I don't think it necessarily is, even though it commonly persists after infarct completion), but that tracing still seems to exhibit an exceptionally, almost agreesively poor R-wave progression across the right precordials. I can't help but wonder if there's an old anterior MI or something else muddying the picture.

Maybe I'm spouting crazy talk, because the paper contains some real heavy-hitters in the field of electrocardiography – Wellens and Bayes jump out at me – but it's still something I'd like to consider. Thanks again for the great case!

Dr. Walsh, could you explain to as why the last ECG of this article showing the typical posterior MI, was not also considered to be an inferior MI? It appears that there is elevation in II, III, and AVF; although, there is less elevation in II than in III, would it not also meet MI criteria for Inferior involvement?

Congrats to those who read the whole discussion – it ended up being a bit long!
KS – No, I agree, that's an inferoposterior. The authors used the ECG as 1) an example of the acute posterior pattern they're describing, and 2) what some people might consider "minimal" STE in the inferior leads. I agree though – the inferior leads look pretty diagnostic, certainly good enough to activate!
Only 10% of AMI presents as an isolated posterior infarct, so there won't be too many "perfect" examples of the isolated and acute pattern.
Vince –
Sending you a copy by FB message! You have some interesting thoughts on the R/S, etc., and I have to keep my eyes open for this aspect. Frankly, all the recent ECGs I've seen w/ posterior involvement have been subacute/old, so I can't speak to the hyperacute/acute pattern in terms of my own experience or research. (I'm not an ECG god, but I know where to read what the gods publish).
Again, I'm not sure that last ECG is supposed to be quintessential, but at least a pretty good example. The IRA in that example was the LCx, BTW.
Send me the link to your online stuff – I'll add it to my sidebar. Plus, I always like me a good ECG blog!

Ken Grauer58 Year Old Male, Workout Worry@ Eli — I don’t see AFlutter. That is, I see no indication of regular atrial activity at a rate consistent with AFlutter. Instead, the rhythm is irregularly irregular without P waves = AFib at a controlled ventricular response. In my opinion, one doesn’t need Sgarbossa criteria here to activate the cath lab. So, yes the…
2018-09-13 02:09:24

Vince DiGiulioIs epinephrine harmful in cardiogenic shock?Sorry about that; I copied the quote from the article and my browser automatically changed the "μ" to an "m". Thanks for noticing, and thanks for pointing it out in the most passive-aggressive manner possible.
2018-09-12 16:45:26

Ken Grauer, MDElectrocardiographically Silent High Lateral STEMI EquivalentHi Tom. This is a great case — so NICE that you posted it for others to learned from. But as I commented several times when you sent this case around to our group — the T waves in V2,V3 are disproportionately peaked and transition occurs early (between V1-to-V2) — so the chest leads are NOT…
2018-08-14 08:38:03

Eli58 Year Old Male, Workout WorryAnybody else see the possibility of a LBBB or A-Flutter? I'm not sure if this will make any difference with the treatments but im just trying to interpret it first because if there is a LBBB then it does not meat Sgarbossa criteria and if it is A-Flutter that could explain the hyper acute T's…
2018-07-20 21:29:21